Linked Life Data

10475095

Source:http://linkedlifedata.com/resource/pubmed/id/10475095

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-10-13
pubmed:abstractText
Confluent monolayers of primary endothelial cells display a high viability and an apparently constant cell density. However upon prolonged cultivation the monolayer degenerates with increasing numbers of senescent cells finally representing the whole culture. Recently we showed that lack of hemodynamic forces induces apoptosis in organ cultures as well as in confluent monolayers of human umbilical cord vein endothelial cells (HUVEC). The apoptosis started at a low level and was counteracted by a continuous proliferation of the remaining cells. Here we show that the induction of apoptosis by lack of hemodynamic forces is a general characteristic of vascular endothelial cells, valid for endothelial cells from various organs and species: human umbilical cord vein endothelial cells (HUVEC), human microvascular placental endothelial cells (HPEC) and bovine aorta endothelial cells (BAEC). Furthermore apoptosis due to the lack of hemodynamic forces can also be induced in various endothelial cell lines: EA.hy 926 derived from HUVEC and PBMEC-A1 derived from PBMEC. However degeneration of confluent monolayers does not occur with these cell lines even in monolayers kept for several weeks. This indicates that the degeneration of normal endothelial cell monolayers is caused by depletion of the proliferation potential of the endothelial cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1062-3329
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
325-34
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Apoptosis induced by lack of hemodynamic forces is a general endothelial feature even occuring in immortalized cell lines.
pubmed:affiliation
TU-Darmstadt Institut für Biochemie, Germany.
pubmed:publicationType
Journal Article